Key result
Patients with prosthetic heart valves and cerebrovascular events had significantly higher levels of platelet microparticles (4.1% vs 2.4%; P<0.05) and microembolic signals than those without events.
Why the study?
Are increased microembolic signals, platelet microparticles, and procoagulant activity associated with cerebrovascular events in patients with prosthetic heart valves?
Case-Control (n=26)
Are increased microembolic signals, platelet microparticles, and procoagulant activity associated with cerebrovascular events in patients with prosthetic heart valves?
Increased microembolic signals, platelet microparticles, and procoagulant activity may explain the occurrence of cerebrovascular events in patients with prosthetic heart valves despite adequate anticoagulation.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for platelet microparticles as cerebrovascular risk markers in prosthetic valves; prospective trials required before clinical adoption.
BACKGROUND AND PURPOSE: Cerebrovascular events (CVE) in patients with prosthetic heart valves (PHV) have remained a severe and frequent complication despite oral anticoagulation with or without aspirin. We studied the possible pathophysiological involvement of platelet-derived microparticles (PMP) as a contributing factor for the increased incidence of CVE in patients with PHV. METHODS: We compared in a retrospective, case-control study the clinical outcome after the implantation of the PHV with several different independent morphological and functional methods, including simultaneous transcranial Doppler monitoring of both middle cerebral arteries, PMP detection by flow cytometry with use of platelet-specific antibodies, coagulation markers, and determination of the procoagulant activity by Russell's viper venom time, a phospholipid-dependent coagulation assay. RESULTS: Eight of 26 patients with PHV had 9 CVE during 136 person-years of observation. Transcranial Doppler monitoring revealed an increased frequency of microembolic signals recorded over a 30-minute period in patients with CVE (75+/-25; median, 55; range, 27 to 248) compared with those without CVE (23+/-12; median, 7; range, 0 to 153; P<0.05) or with control subjects (0; P<0.001). Flow cytometry analysis showed increased levels of PMP in patients with compared to those without CVE (4.1+/-0.6% versus 2.4+/-0.4% of all fluorescence-positive events gated; P<0.05). Increased procoagulant activity was documented by the shortened Russell's viper venom time expressed as an increased level of platelet equivalents per microliter of plasma in patients compared with control subjects (+24.7+/-14.9%; P<0.01). Subgroup analysis revealed that patients with CVE had a higher excess of platelet equivalents per microliter of plasma than patients without CVE in relation to the controls (+68.7+/-36.7%; P<0.05). Mildly elevated thrombin-antithrombin III complexes (2.9+/-0.7; median, 2.3; normal, <2.0 microg/L) suggested incompletely suppressed thrombin formation, and fibrin generation (fibrinopeptide A) was in the upper normal range (2.1+/-0.2; median, 1.8; normal, <2.0 ng/mL), despite adequate anticoagulation (INR=3.6+/-0.1). CONCLUSIONS: Our data show increased microembolic signals, platelet microparticles, and procoagulant activity in symptomatic patients with PHV and provide a potential pathophysiological explanation of CVE.
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Geiser et al. (1998) conducted a case-control in Prosthetic heart valves (n=26). Cerebrovascular events (CVE) vs. Patients without CVE was evaluated on Platelet-derived microparticles (PMP) levels (% of all fluorescence-positive events gated) (p=<0.05). Patients with prosthetic heart valves and cerebrovascular events had significantly higher levels of platelet microparticles (4.1% vs 2.4%; P<0.05) and microembolic signals than those without events.
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